Post-Ischemic Pathophysiology in the Gerbil Brain — Changes of Extracellular K+ and Ca++
It is increasingly recognized that following temporary ischemia cerebral tissue damage may further progress. A protracted development of ischemic injury has been described as “maturation” phenomenon (Ito et al., 1975; Klatzo, 1975). One of its features appears to be the direct relationship between the intensity of the insult and the rate of maturation. A similar relationship has also been observed following recirculation employing biochemical and other parameters (Klatzo, 1975). Irrespective of unequivocal evidence indicating progression of ischemic tissue damage after recirculation, it remains largely obscure which factors are essential and which are merely coincidental. It is also apparent that the selective vulnerability of various brain tissue elements may considerably influence post-ischemic pathology. In order to obtain further insight into the role of the different factors operative in post-ischemic pathophysiology, a model of short-lasting cerebral ischemia was used in which a protracted unfolding of various pathophysiological events could be expected.
KeywordsCerebral Ischemia Regional Cerebral Blood Flow Mongolian Gerbil Selective Vulnerability Spontaneous Action Potential
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